Myristoylation Alters Retinoic Acid-Induced Down-Regulation of MARCKS in Immortalized Hippocampal Cells

Wang, Le; Watson, David; Lenox, Robert H.

doi:10.1006/bbrc.2000.3430

Cited by 9 publications

(6 citation statements)

References 43 publications

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“…Administration of lithium causes the downregulation of MARCKS in rat hippocampus (Lenox et al 1992), and in immortalized hippocampal cells (Watson et al 1994;Watson and Lenox 1996;Wang et al 2000), suggesting a relationship between bipolar disorders and alteration in MARCKS. Although MARCKS has been studied in postmortem brain of suicide victims (McNarmara et al 1999), there have been no studies of MARCKS in patients with bipolar or unipolar disorders.…”

mentioning

confidence: 96%

Protein Kinase C and Phospholipase C Activity and Expression of Their Specific Isozymes Is Decreased and Expression of MARCKS Is Increased in Platelets of Bipolar but Not in Unipolar Patients

Pandey

Dwivedi

SridharaRao

et al. 2002

Neuropsychopharmacology

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Phospholipase C (PLC) and protein kinase C (PKC) are important components of the phosphoinositide (PI) signaling system. To examine if the abnormalities observed in the PIdrolysis of the substrate, phosphatidyl inositol 4,5-bisphosphate (PIP 2 ), by the enzyme phospholipase C (PLC), resulting in the formation of two second messengers, inositol 1,4,5-trisphophate (IP 3 ) and diacylglycerol (DAG) (Berridge and Irvine 1989). IP 3 stimulates the release of intracellular calcium from the endoplasmic reticulum, and DAG stimulates the enzyme protein kinase C (PKC) (Nishizuka 1992), which is one of the major intracellular mediators of signals generated by the stimulation of cell surface receptors.Several studies indicate abnormalities of the PI signaling system in patients with unipolar or bipolar disorders. It has been reported that the hydrolysis of PIP 2 by several agonists, such as sodium fluoride (NaF) and GTP ␥ S, is altered in the postmortem brain of depressed Pacheco et al. 1996). PI signal transduction determined by serotonin (5HT)-, thrombin-, and NaF-stimulated IP formation has also been reported to be increased in platelets of depressed patients (Mikuni et al. 1991;Karege et al. 1996). These abnormalities may be related to abnormalities in receptors, such as 5HT 2A , 5HT 2C , muscarinic M 1 and M 2 , or ␣ 2 adrenergic receptors linked to the PI signaling system or to abnormal levels of substrates, such as PIP 2 , or to components of the signaling cascade, such as G-proteins, PKC, or PLC. Abnormalities in 5HT 2A (Pandey et al. 1995), ␣ 2 adrenergic receptors (Pandey et al. 1990), G-proteins (Garcia-Sevilla et al. 1997Karege et al. 1998;Gurguis et al. 1999), and levels of PIP 2 , a substrate for PI-PLC (Brown et al. 1993;Soares and Mallinger 1996;Soares et al. 1999), have been reported in platelets of unipolar and/or bipolar patients. PLC and PKC are two crucial components of the PI signaling system. Both PKC and PLC have been shown to be involved in a variety of physiological functions, such as synthesis, release, and reuptake of neurotransmitters, neuronal development, transcription, longterm potentiation (LTP), and behavioral responses (Nishizuka 1992). Although the role of PLC in affective disorders has not been fully investigated, some studies have shown abnormalities of PLC in depression and suicide Pandey et al. 1999). On the other hand, very few studies have examined the role of PKC in bipolar or unipolar disorders, although PKC has been implicated in the pathophysiology of bipolar disorders. For example, it has been reported that PKC activity as well as translocation of PKC from cytosol to membrane are increased in platelets of bipolar patients and that lithium treatment alters the activity of PKC in platelets (Friedman et al. 1993;Wang et al. 1999). Further evidence for the involvement of PKC in bipolar disorders is derived from observations that lithium exerts significant effects on PKC in a number of cell systems, including central nervous system (CNS) (Manji et al. 1993(Manji et al. , 1995Manji ...

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mentioning

confidence: 96%

Protein Kinase C and Phospholipase C Activity and Expression of Their Specific Isozymes Is Decreased and Expression of MARCKS Is Increased in Platelets of Bipolar but Not in Unipolar Patients

Pandey

Dwivedi

SridharaRao

et al. 2002

Neuropsychopharmacology

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“…Both these proteins have been implicated in the pathophysiology of mood disorders (Dean et al 1997; Lenox et al 1992; Manji et al 2000; Pandey et al 2002b; Wang et al 2000; Watson et al 1994). The levels of MARCKS have been studied in subjects with mood disorders, and the results suggest that the level of MARCKS may be altered in platelets of patients with bipolar disorder (Pandey et al 2002b).…”

Section: Receptor-linked Signaling System In Suicidementioning

confidence: 99%

Neurobiology of adult and teenage suicide

Pandey

2011

Asian Journal of Psychiatry

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“…Both of these proteins have been implicated in mood disorders [255,256,[262][263][264]266]. Because of the decrease in PKC, there may be altered phosphorylation of one or more of the proteins, which could cause changes in phospho-proteins, such as phospho-MARCKS, and which may cause changes in behavior.…”

Section: Protein Kinase C In Suicidementioning

confidence: 99%

“…A number of growth hormones and pharmacological agents, including phorbol esters, that activate PKC have been shown to phosphorylate MARKS, thereby regulating a number of physiological functions, such as signal transduction and neurotransmitter release [275,276]. Since PKC abnormalities have been implicated in the pathophysiology of mood disorders [263][264][265][266] and suicide [277,278], the levels of MARCKS have been studied in subjects with mood disorders [255]. The results of this study suggest that the level of MARCKS may be altered in platelets of patients with bipolar disorder.…”

Section: Myristoylated Alanine-rich C Kinase Substrate (Marcks) In Sumentioning

confidence: 99%

Monoamine Receptors and Signal Transduction Mechanisms in Suicide

Pandey¹,

Dwivedi²

2006

CPSR

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Suicide is a major public concern and in the teenage population it is the third leading cause of death. Its neurobiology is not well-understood, but recent postmortem brain studies have provided greater understanding of the neurobiological abnormalities associated with suicide. Earlier postmortem brain studies focused on monoamine receptor subtypes, namely, serotonin, e.g., (5HT) 1A , 5HT 2A , and adrenergic receptors. Later, various components of the signaling cascades to which these receptors are linked were examined; 5HT 2A or 1 -adrenergic receptors are linked to the phosphoinositide (PI) signaling system, and -adrenergic receptors are linked to the adenylyl cyclase (AC) system. These studies revealed abnormalities in the components of the signaling systems: G proteins, the effectors phospholipase C (PLC) and AC, or second and third messengers systems, such as protein kinase C (PKC) and protein kinase A (PKA). Further studies found that downstream transcription factors, such as cAMP-response-element-binding protein (CREB), were also affected. Here we critically review the studies, focusing primarily on monoamine receptors and the components of PI and AC signaling cascades in suicide, primarily in postmortem brain. These studies provide a better understanding of the pathophysiological abnormalities associated with suicide and may lead to new therapeutic agents targeting specific sites in the signaling cascade.

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Myristoylation Alters Retinoic Acid-Induced Down-Regulation of MARCKS in Immortalized Hippocampal Cells

Cited by 9 publications

References 43 publications

Protein Kinase C and Phospholipase C Activity and Expression of Their Specific Isozymes Is Decreased and Expression of MARCKS Is Increased in Platelets of Bipolar but Not in Unipolar Patients

Protein Kinase C and Phospholipase C Activity and Expression of Their Specific Isozymes Is Decreased and Expression of MARCKS Is Increased in Platelets of Bipolar but Not in Unipolar Patients

Neurobiology of adult and teenage suicide

Monoamine Receptors and Signal Transduction Mechanisms in Suicide

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